Dexamethasone Does Not Inhibit Treadmill Training-Induced Angiogenesis in Myocardium: Role of MicroRNA-126 Pathway

Area of Science:

• Cardiovascular physiology
• Molecular biology
• Exercise science

Background:

• Dexamethasone (DEX) exhibits anti-inflammatory effects but can induce hypertension and skeletal muscle microvascular rarefaction.
• The impact of DEX on cardiac microcirculation remains largely unknown.
• Exercise training is known to prevent microvessel loss in skeletal and cardiac tissues by modulating microRNA expression and angiogenic/apoptotic protein balance.

Purpose of the Study:

• To investigate the effects of dexamethasone and/or exercise training on cardiac microcirculation.
• To determine if DEX or exercise training induces alterations in microRNAs related to cardiac angiogenesis or microvascular rarefaction.

Main Methods:

• Animals underwent 8 weeks of exercise training and received subcutaneous dexamethasone (50 μg/kg/day) for 14 days.
• Cardiovascular parameters were monitored.
• Left ventricle tissue was analyzed for microvascular density, microRNA expression, and protein levels.

Main Results:

• Dexamethasone administration increased arterial pressure but did not lead to cardiac microcirculation rarefaction.
• Treadmill training effectively prevented the dexamethasone-induced rise in arterial pressure.
• Exercise training, independent of dexamethasone, upregulated microRNA-126, phospho-protein kinase B/protein kinase B, and endothelial nitric oxide synthase, promoting cardiac angiogenesis.
• Dexamethasone alone did not alter capillary density or inhibit exercise-induced cardiac angiogenesis.

Conclusions:

• Treadmill training stimulates myocardial angiogenesis through enhanced angiogenic pathways and increased microRNA-126 expression.
• Dexamethasone does not induce capillary rarefaction in the heart and does not interfere with exercise-induced cardiac angiogenesis.